We have recently discovered that the contractile elements of the myocardium contain a viscoelastic element which provides a length independent restoring force to the muscle. This element enables the ventricle to store some of the energy liberated during contraction, and use the energy to hasten diastolic relaxation. It also greatly complicates studies of the mechanical properties of heart muscle. To overcome this complication, we plan to make a "striation follower" that will enable us to measure, and control in a servo-system, the length of a central segment of isolated cardiac muscle. Servo-controlled length steps will be applied to both stimulated and relaxed papillary muscles. The force responses of the relaxed muscle will be subtracted from the responses of the stimulated muscles to define the tension transients produced by the cross-bridges formed during contraction. In addition, the calculated increases in force in the passive elements during isotonic shortening will be calculated to obtain an accurate estimate of the force-velocity capabilities of the cross-bridges. The corrected tension transients and force-velocity relations will be measured during various inotropic interventions to determine whether any of the interventions influence the actomyosin cross-bridges directly, or whether all inotropic interventions act simply by increasing activation of the thin filaments. The inotropic interventions include increased stimulation rate, pair pacing, cardiac glycosides, epinephrine, and caffeine. The proposed analysis will attempt to distinguish between the four following reactions in the cross-bridge cycle: 1) attachment of bridges; 2) movement of attached bridges; 3) detachment of bridges; 4) recovery of recently detached bridges. In addition, the rate of rise of thin filament activation will be inferred from the rise of extrapolated isometric force. This value is determined by extrapolating force-velocity curves, measured during the rise of activation, to zero velocity. The results should provide more accurate data to design better tests for rassessing ventricular contractility and more rational clinical therapies.